Temporal acuity and dilation are explored by analyzing firing rates of 2 common glutamate receptors. A phenomenon known as visual strobing often occurs on drugs that interact on the glutamate NMDAr and AMPAr receptors, which can be compared to stroboscopic vision. Actual stroboscopes are also capable of inducing psychedelic geometry in a frequency-dependent manner. The flicker of strobe lights can be compared even to audio waves, which ripple like waves on liquid surfaces, essentially producing something analogous to a stroboscope. The patterns generated by audio frequencies in a liquid medium appear to match the geometry produced by strobe lights at the same frequencies. Video examples are shown along with a video that allows you to experience the patterns for yourself.

Temporal acuity

Both NMDAr and AMPAr are glutamate receptors and are involved in sensory processing (among much more). NMDAr produces slower signals while AMPAr are generally far faster and first to fire. AMPAr seem to fire in the 10ms range and NMDAr in the 100s of ms range, according to some PhDs on quora, with AMPAr being as quick as 1ms according to Wikipedia. I am struggling to find exact numbers in studies so please comment below if you have these studies. The slow rate of firing for NMDAr is perfectly suited for automation (learning). It is low resource wasting, low energy, and allows the maintenance of hyper-familiar functions to go without significant efforts. On the other hand, the quick rate of AMPAr signaling would allow you to keep track of acute details, allowing you to fully analyze and process whatever relevant signals will become associated to each other, forming new automations that eventually become NMDAr mediated as well.

It might be that the ratio of AMPAr:NMDAr is determined by the necessity of temporal acuity for any given process. Some signaling would require sensitivity to more acute changes, where the default state for unfamiliar signals would be hyper-acuity until the necessary degree of acuity is determined, at which point irrelevant signaling can be shut out, reducing acuity. AMPAr would be first to downregulate upon repeated neuron stimulation with glutamate because it is firing more often, at which point NMDAr dominance begins and the ratio of AMPAr:NMDAr would be dependent on the frequency of neuron stimulation ultimately. To simplify, NMDAr will outlast while AMPAr will fall faster. High acuity temporal events would not typically fall under the umbrella of longer exposure of stimuli, unless the stimuli was very repetitious which may make the stimuli predictable, automatable, and irrelevant to acute attention. If a behavior can respond to a predicted event and operate within 150ms time pixels then it will be highly NMDAr dominated due to AMPAr becoming overused and downregulated. AMPAr on the other hand would dominate during novel circumstances, which allows acute awareness so that significance of stimuli can be sorted. There is some evidence of this NMDAr/AMPAr ratio involvement in temporal acuity in this study here. It talks about the difference in firing rate for AMPAr compared to NMDAr and how NMDAr is involved in summating temporal events. The concept is intitially inspired by mechanisms of Long Term Potentiation (LTP), which you can introduce yourself to here.

It seems to be that while watching the repetitious spiral motion in this video below, our brain goes from this acute awareness to the more automated state (from AMPAr dominance to NMDAr dominance and LTP), demonstrating this effect in action. Once the video stops, you perceive continued automated perceptions of motion for some time, possibly indicating Long Term Potentiation. Check out The Sanity Illusion to see my argument that these sort of illusions are mediated by NMDAr partly, but for now let’s continue on.

Seizure warning, be careful.


When I first tried cannabis I took a massive amount, expecting I would never return to the substance. When I first dosed the cannabis it took seemingly 40mins for my NMDArs to downregulate and allow AMPAr to dominate signaling, as this is when dissociative tripping began. This moment was total insanity. When you break the automation of the most fundamental aspects of being human, this is when experience gets truly absurd. You begin to see the flicker. And it is a horrifying state of mind, the darkest most profound state of awe.

At first one might assume this is the flicker of reality, that this is some kind of evidence for our existence within a simulation. You might assume it is the flicker of your own consciousness being observed from some distance. But you may be like me, and wonder if it could be the flicker of the lights in the room. The walls pulsating rapidly, everything appears so strangely disconnected, yet also simultaneously and paradoxically complete and organized. Movement appears in a surreal clarity, without the blurs of motion, and in an almost musical pattern. If blurs exist they appear as object duplicates sometimes or a hyper-vivid stream of the moving object. The walls pulsate so rapidly and everything in the room appears like an old-television screen.

See the source image

The switch to AMPAr dominance in visual processing would theoretically enhance acute temporal intake of visual information which allows you to see temporal events that are typically too acute to perceive. Namely the flicker of lightbulbs that is elusive to our perception while sober. Incandescent and fluorescent lightbulbs flicker at twice the frequency of AC, according to this article, which also states that common 100-120Hz flickers are known to cause effects in humans such as migraines, even when imperceptible. If it’s true that AMPAr signals can rise and fall at frequencies of 1ms or even in the 10ms range, AMPAr hyper dominance would be a sufficient level of acuity to process temporal events occurring in the 100-120Hz range. If AMPAr signals at 1-10ms, this means the acuity of signal response is as high as 1000Hz but more likely this is too extreme so we should assume its less than this. With NMDAr we might expect 100Hz signaling or less.

Another possibility is that with NMDAr cut out of the picture, AMPAr may not transmit a smooth uncut image and so the flicker may be AMPAr transmission unaided by NMDAr which may aide in smoothing the signal and filling gaps, essentially the previously described summation of temporal events. Perhaps AMPAr domination results in the loss of summation, something opposite of palinopsia (visual trailing), which may be an NMDAr dominance effect. This flickering effect appears to occur on NMDAr antagonists as well, where it has been described as stop-motion, flanging, and strobing. In this sense, it could be you observing the altered frame rate of consciousness via a lens of higher frame rate area of perceptual processing. 

It’s possible to test the hypothesis involving lightbulb flickers. An easy way would be to have alternating frequencies in light bulbs, checking if a person in this cannabis intoxicated state notices the change in frequency. Lastly, we may see both of these hypotheses being true. We should also check if there are any reports of strobing occuring outdoors in sunlight, which I assume is a rather rare context for dissociative anesthetic intoxication outside of PCP in Florida.

Looking into the maximum temporal acuity of our visual perception I found that events as short as 13ms can be perceived, topping a previous 100ms record. Going even further, during saccades it has been recorded that events occurring in the 2000Hz ranges could be detected consciously, while 3000Hz surpassed recognition, becoming invisible. Another study showed that observations could occur in the 500Hz range of flickering lights. Saccades may invoke AMPAr stimulation due to the sudden higher demand of temporal acuity from the rapidly changing visual scene, thus increasing the frequency of information processing to compensate. 

Saccades are of particular interest here as cannabis is known to affect these processes. As cannabis is known to induce psychosis (even temporarily in mentally healthy individuals), it’s worth noting that saccades are affected in the same way for schizophrenic patients. A major theory of schizophrenia is NMDAr hypofunction, and cannabis is thought to be capable of inducing this. The interactions between CB1 and NMDAr seem complex, but generally may reduce NMDAr function. The narrative for cannabis’ general effects is also complicated, involving even a suppression of AMPAr activity

Strobe lights are capable of inducing geometric visual patterns much like psychedelics. If you would like to test this, try this video:


I’ve personally found that this stroboscope effect produces not only honeycomb visual geometry, but color morphing, and even motion after-effect style visuals if I watch long enough. There are actually theories that explore stroboscopic mechanisms of psychedelic effects. The stroboscope in the linked video oscillates at 12Hz, which means it gets close to 83ms acuity range. This may begin to pressure AMPAr signaling and speed up glutamate release cycles, potentially causing seizures, auras, and migraines. The increased glutamate release may emulate some of the effects of psychedelics because this is a key mechanism of psychedelic effects. We will come back to psychedelics a bit later and go in more depth. 

The patterns of water made by strobing waves, isn’t that all audio is?

Notice especially towards 12 seconds of the video below, you’ll realize those are the same sort of patterns induced by the strobing video at 12 Hz. It is fascinating. As the frequency increases, it begins to look more like the visual distortions caused under the effects of cannabis.

Background Noise

Have you ever heard that listening to a song while studying, and replaying this song while testing allows better recall due to context-dependent memory? We often don’t consider that while in a dream, reality is as hard to remember in the dream as the dream is to remember while awake. This seems to be evidence of an ubiquitous context that exists in our mind while awake, that dissolves while we sleep. I believe that we remain in a conditioned state as we leave childhood that we tie most of our waking memories to. A sort of mental soundtrack to our lives, a stability that allows a universal context to associate new memories more quickly and aide in faster learning. Gravity, certain smells, the blue sky, the shifting of time that dictates the cycles of day and night, your own body, and your conception of the world, would be examples of omnipresent cues. It is this context that is absent in dreams, but also in altered states of mind that makes thinking so different and recall of context-associated memories so difficult. Dreams and states of serious cannabis, psychedelic, or dissociative intoxication may be exceedingly difficult to remember because we cannot cue these memories in sober states as easily. It is like the child who sees the world with novelty intact. These states can allow us to come across novel reinterpretations of reality that we find valuable and life altering. It could be that the purpose of sleeping is to prevent excess desensitization of the background context in order to prevent something like psychosis. There is some evidence that chronic low-grade sleep deprivation leads to NMDAr desensitization, which is linked to psychosis.

Our universal context likely makes it difficult to experience gestalt shifts of perception, a sort of grounding agent that connects many associated rudimentary sub-object perceptions. Things such as dimensionality, shape recognition, and modular aspects of object-recognition. Imagine that corners are a recognized sub-object memory. The core of these memories would be the hippocampus, where seizures often induce auras and illusions, and as the storm of glutamate activity spreads, sensations of dejavu are experienced as the universal context is enhanced. Everything rapidly becomes ever-lucid and familiar. It could be that recall of the immediate present moment occurs simultaneously with experiencing it, a sort of remembering as it is happening effect, in which learning becomes super-enhanced by the flood of glutamate that swarms neurons, accelerating the learning process to the point that it is instantaneously learned, recalled, and then overstimulated to the point of cell death (in seizures). 

Into the hole we go.

See the source image


NMDAr antagonists on the other hand appear to have an opposite effect, revoking access to the universal context, disintegrating object recognition and inducing the opposite of dejavu, amnesia. On strong doses, the suddenly unfamiliarized perceptions can appear like rorschoch tests, but far less blobby, and much more of a baroque-style intricacy.

Unfamiliarization – The objects in the image below almost appear familiar yet they seem completely unrecognizable. The meme was spread around recently with titles like ‘Name One Thing In This Picture’. This resonates with the clutter unfamliarity of dissociative experiences, similarly struggling to recognize and define the objects around me.


As I view myself in the mirror on NMDAr antagonists, I find that every angle of view upon my face looks as if I am viewing a multitude of different people. There is a clear lack of continuity and rotating my perspective appears as if it is morphing incoherently, while holding still appears to create a stable experience. There is a profound stillness that I find exists in these states, a sense that nothing is alive until it begins to move. This also used to occur after prolonged periods of taking the medication Adderall, which is known to upregulate NMDAr antagonist mechanisms.

My face when I rotate my head in the mirror to observe all angles on NMDAr antagonists.

See the source image

An effect of dissociative anesthetics that overlaps with another NMDAr disrupting substance, alcohol, is saccadic ghosting. When you turn your head, duplications of stimuli seem to occur on these drugs. Have you ever panned your visual field across a scene with a digital clock? The displays on these clocks often will appear to be split into individual duplications. You can observe this by vibrating your eyes while looking at a digital clock, the effect is apparent. The flickering of the digital clock reveals itself during these saccadic movements and ghost images appear and disappear rapidly. On alcohol or anesthetics, turning your head produces a choppy experience, sometimes perceptions of spinning also occur. The saccadic ghosting on anesthetics unveils the strobing nature of your entire visual field.

As the anesthesia of NMDAr antagonists wears off, there is many distinct perceptual effects. The walls morph and move, there is a lot of visual motion, seemingly due to the restoration and hypersentivity of NMDAr dependent summation processing. The motion after effect illusion becomes prominent upon coming back up to sensory baseline. I liken this to the numbness one can experience in the hands from extreme cold or low blood circulation. When your limb regains sensation, there is an experience of tactile white noise or even something akin to phosphenes. Sometimes even a sensation that the body is vibrating can occur. The restoration of many functions that are normally not distinguished in daily life due to their everlasting presence causes fascinating white-noise perceptual and cognitive equivelents, and illusions begin to colonize your perceptual experience as NMDAr function is restored, and likewise the relatively proesthetic baseline.


The essence of the dissociative experience is degradation of sensory and cognitive processes and then later a hypersensitive restoration of these processes. Psychedelics take on a different pattern, one that is hard for me to parse still. One notable aspect of psychedelic drugs is their ability to disinhibit glutamate release and consequently induce pro-esthetic effects or a state of pro-esthesia (opposite of anesthetic/anesthesia, but also to mean beauty enhancing as well).

Look primarily at the origin section.


5HT2a agonism, the primary mechanism of the serotonergic psychedelics, induces glutamate release through 5HT2a-mGlu2 heteromers, which is thought to be behind the perceptual effects of the drugs. The release of glutamate would enhance both NMDAr and AMPAr signaling, but the relationship these mechanisms have with the glutamate system is rather complex. One study claims that common psychedelic 5HT2a partial agonists have only a partial agonist relationship to NMDAr, so its possible that the very low doses we use for many of them are producing mostly agonistic effects, but upon higher dosing we may see antagonistic patterns similar to dissociative drugs, albeit by an entirely different mechanism. Although it seems that most accounts of the effects of psychedelics appear to be agonistic of glutamate in general. 

NMDAr antagonists reduce incoming signals, while NMDAr, AMPAr, and general glutamate enhancers would produce extra signaling, potentially regardless of incoming stimuli, but also modulating incoming stimuli. If the effects of dissociative anesthetics are to diminish senses, induce strobing effects, saccadic ghosting and also reduce some of the NMDAr dependent illusions, then we would see the psychedelic proesthetics having much the opposite effects, enhanced sensory experience, palinopsia (opposite to saccadic ghosting), blending of temporal events, and enhanced development of illusions such as the motion after-effect. 


Psychedelics seem to cause a sort of enhancement of the universal contexts while also breaking the dependency upon and alleviating the involuntary nature that these contexts seem to have. This allows a mental freedom, to allow gestalt reanalysis of existence under various reinterpretations of memory data and present stimuli without complete dissociation or amnesia that comes with NMDAr antagonists. A similar reinterpretation may occur under dissociative drugs but with much more present stimuli focus, with the combination of deleterious perceptions that fade due to the anesthetic and amnesiac nature of these drugs. Although earlier stages of NMDAr antagonist intoxication also boosts glutamate release which would have paradoxical effects compared with the later stages of intoxication when many NMDAr are occupied by the antagonist.

While NMDAr antagonists produce a discontinuous and more disrupted visual experience, psychedelics seem to add layers that were previously numb, producing the same kind of sensory tingling that occurs when we thaw our frozen hands in warm water. With pro-esthetics there is a sort of hypercontinuity to things, everything is flowing together, you are rapidly learning and dissolving, simultaneously evolving and rebirthing like a phoenix, rising and falling with this diminished sense of assumingness about the world, but not a complete loss, which allows for more informed remolding of perspectives compared to dissociative anesthetics, which completely block out assumingness altogether (dose dependently of course), bringing one back to childlike ignorance and a supreme state of mystery and novelty.

Temporal Dilation

This AMPAr:NMDAr concept could even explain the exaggerated slowness of time that is experienced under these hallucinogenic-induced states as we would expect temporal acuity itself is a stretching of time awareness. It is probable that the brain attempts to minimize acuity of temporal awareness as much as possible in order to maximize energy efficiency and also reduce the amount of conscious information, making it easier to process the world around us.  

It’s not apparent that temporal acuity is what causes the experience of time dilation, but perhaps a profound immersion into the present moment that leaves behind awareness of time passing, or even both. Normally we are so familiarized with the repetitious existence of our adult lives, only fleeting unpredicted events capture our attention, sudden loud noises may induce a very temporary state of flow, a sudden halting of our background mental chaos, a sharp focus of the event in order to fully understand what is occurring. The child on the other hand, may live in an endlessly loud and chaotic environment of confusion and awe. 

D2 dopamine receptors are implicated in flow, where research has shown that increased D2 density correlates with flow state proneness. People often use stimulants to induce flow-like states but with diminishing returns as D2 receptors downregulate in long-term users of the drugs, a pattern that even occurs with heavy internet users. Those who seek novelty will probably be the first to run out of novelty and begin their journey on an endless treadmill of boring, predictable stimuli. Users of Instagram are likely trapped in flow states, just cycling through endless amounts of content, downregulating these mechanisms and also desensitizing them to novel stimuli in ordinary life.

Flow style immersion is valuable when assessing the unfamiliar, un-automated, and the supremely novel. As stimuli becomes familiarized, temporal acuity is reduced to match the necessity of its utility for automating the acquisition of rewards and security. We only need to be aware of what is necessary to repetitiously exploit the stimuli and automate our behavioral response to it. In the past I’ve written about the function and mechanisms of the D2 receptor in Pavlovian Prisons. In a sense, the D2 receptor may function by halting the automation of attention which is typically mediated by sequences of D1 and NMDAr signaling pathways and induce enhanced perception through heteromeric interactions with 5HT2a-mGlu2 receptor signaling cascades, increasing glutamate, ultimately boosting perception and attention to the present moment. 

The true purpose of the flow state is to allow us to maximize our ability to collect the coincidences that structure our entire sense of understanding about the universe and all of its nuances. 


A concept that clearly relates to this temporal acuity concept is the popular coincidence detection notion. The longer time a signal is persisting, the more overlap with other signals it can have, opening the window of time that coincidence can occur. The D2 receptor is said to play a role in coincidence detection, which I’ve outlined a partial role above. It seems to focus our attention towards the immediate experience. According to the study linked above, D1 and D2 receptors have interplaying roles in associative Long Term Potentiation. This study mentions one of the involved mechanisms of D2 receptors is to suppress GABAergic signaling, which supports the temporal dilation concept as GABA predicts time perception.


Brainwaves are often studied, usually with an EEG. They are of particular relevance to this temporal acuity concept because higher acuity perception is based on an increase in neuronal firing frequencies. There are different ranges of brain frequencies as follows:

Theta – 4-8Hz

Alpha – 8-13Hz

Beta – 13-38Hz

Gamma – 38-100Hz

Generally low frequencies are related to calm states, while high frequencies represent intense brain states like stress. Research on Alzheimer’s shows that using strobe lights to entrain the brain to gamma frequencies can eliminate more than 50% of beta amyloid plaques, but shortly after cessation of light therapy, the beta amyloid returns. Beta amyloid functions partly by promoting NMDAr mediated excitoxicity. By rescuing AMPAr signaling we may find that NMDAr is less dominant. Perhaps beta-amyloid has the potential to build up in low frequency brain states. It could be that dynorphin is partially implicated in the slowing of the aging brain, by reducing glutamate activity, and somehow allowing for beta-amyloid to build up. Although this isn’t clear as there is research suggesting that dynorphin could improve cognition when impaired by beta amyloid, while on the other hand another paper suggests dynorphin could be related to cognitive impairment and neurodegeneration involved in Alzheimer’s disease. Since both beta-amyloid and dynorphin are neurotoxic by distinct mechanisms, even having opposing functions on NMDAr, it could be that both are true. During seizures, it is thought that dynorphin may release and function as an NMDAr antagonist, preventing further excitotoxic risk, at the cost of psychotomimetic effects. If this is triggered by NMDAr stimulation, then it could mean beta-amyloid causes a persistent increase in dynorphin, which might further decrease glutamatergic tone and cause amnesiac effects. 

As I continued to research down this rabbit hole, I stumbled upon gems. Every bit of information seemed to effortlessly integrate with the temporal acuity theory. AMPAr antagonists were found to reduce gamma frequencies and increase slow waves, which implies that AMPAr may be required for the high frequency brain activity, as predicted. Furthermore, AMPAkine drugs are being researched as Alzheimer’s treatment. Cannabis also increases lower range gamma frequencies and reduces slow waves, fitting the theory. THC is also being researched in improving memory in age-related cognitive decline. Psychedelics increase gamma frequencies as well but in the higher range of gamma frequencies, as opposed to the lower ranges like cannabis. This study also suggests that ketamine (an NMDAr antagonist) has a larger impact on gamma waves compared to psychedelics, which makes sense as psychedelics still promote NMDAr stimulation, but only partially. Speaking of which, the NMDAr antagonist memantine is being explored for Alzheimer’s disease, and going by these patterns, perhaps psychedelics may prove beneficial as a treatment option for Alzheimer’s patients. 

Psychedelic drugs may be beneficial to Alzheimer’s patients over cannabis and NMDAr antagonists due to the amnesiac tendencies that these two have. The partial agonism of psychedelics may provide a limit on NMDAr activity while allowing it to still be stimulated partially while also boosting AMPAr activity and gamma waves. 

When I was exploring brain waves, something kept bothering me. It was the fact that 100Hz waves barely reach the frequencies of household lights (100-130hz).

And then I came across something else.

Lambda – 100-600Hz (??)

My initial search left me overexcited, every result came up with research on visual processing and saccadic movements. These bizarre underresearched waves are implicated in visual exploration, especially in regards to more complex imagery, and also saccades. Lambda frequencies are implicated in the offset, as opposed to the onset of saccades. It could be that the brain does not bother as much with processing the fine details of constantly changing signals, via the process known as saccadic suppression, but once the eyes rest on some new image, a rapid increase in signaling occurs in order to stabilize the image, fully complexifying it, and populating it with objects. The new resting image would be relatively unfamiliar and complex since shifting your eyes produces an entirely different perspective. It’s worth noting that lambda waves seem to occur primarily or even entirely in perceptual and visual processing regions of the brain, namely the parietal-occipital areas.

As lambda waves are usually seen in children 3-12 years of age, it could be that these waves deal with the unfamiliar images, rapidly assimilating them into the familiar. Although not human, a monkey in a room would experience sudden storms of lambda activity when a human enters the room for the first time, potentially until the person is further understood. That study explores a few different animals’ lambda frequencies, although remember, in humans lambda seems to be strictly perceptual. It isn’t clear if this is true of the animals as well.

Could it be that psychedelics trap you in gamma-lambda frequency states? This would also fall in line with the research comparing the psychedelic state and the state of mind seen in children. As previously mentioned, the anti-glutamatergic mechanism dynorphin upregulates as we get older. Along with glutamate release inhibition, this neurotransmitter is a KOR agonist and NMDAr antagonist. Psychedelics have been shown to attenuate KOR-mediated depressive effects, and so it follows that psychedelics may be able to reverse age-related cognitive changes, which I’ve explored in both Adultification and Psychedelics and Intelligence. Perhaps an aspect of Alzheimer’s disease involves the natural decline of novel and stimulating experiences that occurs in elderly age, an omnipresent hyper-familiarity. On the opposite end, psychedelics may restore the child-like state of mind, with the potential of restoring functioning of the brain that is declining with old age. 

I found a nonscientific source claiming that lambda waves could be involved in tripping effects such as out-of-body experiences. It was a struggle to find much else on this topic, but it would at least make sense if these tripping drugs induce their effects by increasing brain frequency rates a pattern which is also found in bipolar schizoaffective disorder. In both the drug and bipolar schizoaffective studies it suggests an increase in gamma frequencies but unfortunately there are not studies involving lambda frequencies and these topics. There is a post describing visual aura in relation to lambda frequencies, but the page doesn’t detail much about this case. 

My earlier experiences under the effects of cannabis could be made sense of through this perspective. Before tolerance, the effect was an extreme sensitivity to the environment. As the cannabis peaked, my auditory processing notably expanded, as well as my vision. While sitting in a restaurant waiting for food, the sounds of all the machinery and their seemingly mathematical patterns of oscillation became freed from my attentional inhibition. My sense of gravity became overwhelming, as if I would be sick from slight movements, I was falling off of a virtual cliff, back and forth, feeling the liquid move around in my ear. During dinner my peripheral vision became very enhanced, I almost couldn’t tell where the center of my vision was anymore. Every detail of people’s face, the crumbly textures, the red and multicolored patches of skin, the highlights and shading became disturbingly apparent. In an almost paradoxical way I felt nearly blinded by overstimulation and chaos. 

After some amount of tolerance, the visual effect was an enhancement of recognized space, a kind of dreamlike massiveness. I notice this has occurred without the aide of drugs when I first entered large cities such as Los Angeles. The depth of the buildings produced a strange visual effect. After spending sufficient time in the city this seemed to fade and the feeling of cities and suburban areas is no longer that distinct. Cannabis was able to induce an effect like this inside of my room while I was observing objects on my desk. This effect was enhanced by memantine also, but I do not remember if it occurred with memantine alone. Aniracetam was also capable of inducing this, as were psychedelic such as LSD during microdoses. The perception of massiveness might be due to the unfamiliarity and novelty of massive environments such as canyons or large cities, not being a product of massiveness itself, but rather the unfamiliar dimensionality of these spaces, simply something I’ve associated with massive environments because this is when the effect was present. Many of these effects of cannabis reminded me deeply of childhood and brought back memories of perceptual experiences that I remember having in very early childhood.

I suspect that we typically oversimplify spatial awareness after getting a feel for the comparative depth and other attributes of various objects and spaces. After this point, perhaps only extremely novel and unfamiliar environments are capable of re-engaging these higher levels of experience, much like when I first entered the city of LA. Simplifying reality helps reduce the burden of our senses, as processing all of these details is usually not necessary nor helpful. On drugs we may experience the world as if it were novel again by either disrupting familiarity or artificially inducing higher energy states of cognition.

Please share your experiences in the comments below.

I’d especially like to know what you think about these ideas and whether you’ve experienced the strobing effects in particular. Have you experienced strobing outdoors?

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